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Human Lung Cancer Risks from Radon – Part III - Evidence of Influence of Combined Bystander and Adaptive Response Effects on Radon Case-Control Studies - A Microdose Analysis

机译:Rad引起的人类肺癌风险-第三部分-旁观者和适应性反应联合作用对Rad病例对照研究的影响的证据-微剂量分析

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Since the publication of the BEIR VI (1999) report on health risks from radon, a significant amount of new data has been published showing various mechanisms that may affect the ultimate assessment of radon as a carcinogen, in particular the potentially deleterious Bystander Effect (BE) and the potentially beneficial Adaptive Response radio-protection (AR). The case-control radon lung cancer risk data of the pooled 13 European countries radon study ( Darby et al 2005 , 2006 ) and the 8 North American pooled study ( Krewski et al 2005 , 2006 ) have been evaluated. The large variation in the odds ratios of lung cancer from radon risk is reconciled, based on the large variation in geological and ecological conditions and variation in the degree of adaptive response radio-protection against the bystander effect induced lung damage. The analysis clearly shows Bystander Effect radon lung cancer induction and Adaptive Response reduction in lung cancer in some geographical regions. It is estimated that for radon levels up to about 400 Bq m?3 there is about a 30% probability that no human lung cancer risk from radon will be experienced and a 20% probability that the risk is below the zero-radon, endogenic spontaneous or perhaps even genetically inheritable lung cancer risk rate. The BEIR VI (1999) and EPA (2003) estimates of human lung cancer deaths from radon are most likely significantly excessive. The assumption of linearity of risk, by the Linear No-Threshold Model, with increasing radon exposure is invalid.
机译:自BEIR VI(1999)报告发表以来,有关ra的健康风险的报告已经出版,大量新数据表明可能影响ra作为致癌物最终评估的各种机制,特别是潜在的有害旁观者效应(BE) )和潜在有益的自适应响应无线电保护(AR)。评估了13个欧洲国家ra气研究(Darby等,2005,2006)和8个北美血统研究(Krewski等,2005,2006)的病例对照ra肺癌风险数据。基于地质和生态条件的大变化以及针对旁观者效应引起的肺损伤的适应性反应放射防护程度的变化,调和了肺癌与ra风险的比值比的大变化。该分析清楚地显示了某些地理区域的肺癌旁观者效应ra诱导和适应性反应减少。据估计,对于高达约400 Bq m ?3 的ra水平,将不会有30%的人罹患ra的肺癌风险,而有20%的可能性低于below风险。零-,内源性自发或遗传上可遗传的肺癌风险率。 BEIR VI(1999年)和EPA(2003年)对ra引起的人肺癌死亡的估计极有可能过高。通过线性无阈值模型,随着exposure暴露量的增加,风险线性度的假设是无效的。

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